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findings support the hypothesis that TRIB1 gene expression in human umbilical vein endothelial cells depends on the duration of intrauterine exposure to hyperglycaemia
our study reveals that TRIB1 promotes CRC cell migration and invasion by up-regulating the expression of MMP-2 via the activation of FAK/Src and ERK pathways, knockdown of TRIB1 expression in CRC cells abolishes these effects.
role of TRIB1 in cell cycle and survival that is mediated via the modulation of NFkappaB signaling.
the co-operativity observed between MYC and TRIB1 in the absence of PML/RARA show that, outside of acute promyelocytic leukemia, gain of both genes may drive selection for trisomy 8.
The crucial role of TRIB1 in cisplatin-induced enrichment of CSC and drug resistance was verified by knockdown TRIB1. Interestingly, cisplatin treatment also contributed to the increasement of HDAC, the interaction of TRIB1 with HDAC, and inactivation of p53.
Trib1 formed a complex with pHDAC1.
Studies indicate that tribbles homolog 1 (Drosophila) protein appear to be involved in some of the most common diseases, such as cancer, metabolic disease and hyperlipidaemia.
Studies suggest that pseudo-kinase family of tribbles (TRIB) proteins TRIB1, TRIB2 and TRIB3 play roles in pathogenesis of rheumatoid arthritis (RA) and osteoarthritis.
Studies indicate that the minor allele of a single nucleotide polymorphism (SNP, rs6982502) in the regulatory sequence reduces the activity of the tribbles homolog 1 (Drosophila) protein (TRIB1) promoter.
Studies suggest that pseudo-kinase family of tribbles (TRIB) proteins TRIB1, TRIB2 and TRIB3 were involved in the pathogenesis of inflammation.
Studies indicate that tribbles homolog 1 (Drosophila) protein (TRIB1) interacts with the master molecule of Tregs, forkhead box P3 (FOXP3), a transcription factor essential for Treg suppressive activity.
Studies indicate that tribbles homolog 1 (Drosophila) protein (tribbles-1; TRIB1) is an important modulator of human energy metabolism and metabolic syndromes.
Studies indicate that small molecules can reveal rate-limiting signalling outputs and functions of pseudo-kinase family of tribbles (TRIB) proteins TRIB1, TRIB2 and TRIB3 in cells and intact organisms, serving as guides for the development of new drugs.
Studies indicate that overexpression of the wild-type tribbles homolog 1 (Drosophila) protein (Trib1) gene effectively induces leukaemia.
Studies show that TRIB1 and TRIB2 are highly expressed in molecularly-defined sub-types of acute myeloid leukemia (AML).
Studies show a remarkable reduction in tribbles 2 protein (Trib2) expression during oocyte maturation whereas tribbles 1 protein (Trib1) and tribbles 3 protein (Trib3) expression was significantly increased during this process.
SNP rs17321515 associated with plasma triglycerides level and increasing risk of coronary heart disease in male Chinese Han population
These studies indicated that SAP18 expression enhanced the recruitment of mSin3A in coordination with TRIB1 to MTTP regulatory elements and increased MTTP expression.
TRB1 negatively regulates tumor-suppressor activity of p53 through p53 deacetylation
trait-specific genetic risk scores are robustly associated with 10-yr changes in lipid levels and three individual SNPs in APOE, TRIB1, and APOA1 were strongly associated with 10-yr changes in lipid levels
The Liver Clock Controls Cholesterol Homeostasis through Trib1 Protein-mediated Regulation of PCSK9/Low Density Lipoprotein Receptor (LDLR) Axis.
Deletion of hepatic Trib1 leads to increased C/EBPalpha binding near upregulated lipogenic genes, as well as Trib1 itself.
TRIB1 and TRIB3 are more strongly expressed than TRIB2 in cumulus cells (CC) surrounding oocytes from preovulatory follicles than in CC of immature ones.
These data suggested that the modulation of TRIB1 expression affects hepatic lipogenesis and glycogenesis through multiple molecular interactions.
In gene knock-down experiments in macrophages using small interfering RNAs targeted to Trib1, it was observed that TNF-alpha production was increased following treatment with IFN-gamma and/or TLR2 ligands.
These results indicate that COP1 and Trib1 act as an oncoprotein complex functioning upstream of C/EBPalpha, and its ligase activity is crucial for leukemogenesis.
tribbles-1 is a novel binding partner of Foxp3 in regulatory T cells
results demonstrate that Trib1 is critical for adipose tissue maintenance and suppression of metabolic disorders by controlling the differentiation of tissue-resident M2-like macrophages
Trib1-knockout mice showed elevated levels of plasma TG and cholesterol due to increased VLDL production.
Trib1 transduced hematopoietic stem cells developed acute myeloid leukemia.
Dual role of TRB1 as both a target and a (co) activator of inflammatory signaling might provide a molecular rationale for the amplification of proinflammatory responses of adipose tissue.
describe suppression of adipocyte differentiation by TRBs Trib1, Trib2, Trib3
These results demonstrate that Trib1 is a negative regulator of NF-IL6 protein expression and modulates NF-IL6-dependent gene expression in toll-like receptors-mediated signaling.
a nuclear factor\; gene expression induced by m1-acetylcholine receptor
tribbles homolog 1 (Drosophila)
, G-protein-coupled receptor induced protein
, phosphoprotein C8FW
, tribbles homolog 1
, G-protein-coupled receptor-induced gene 2 protein
, G-protein-coupled receptor-induced protein 2
, phosphoprotein regulated by mitogenic pathways
, tribbles-like protein 1
, G-protein-coupled receptor induced protein GIG2